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Prevalence of Plasmodium falciparum pfcrt polymorphisms and in vitro chloroquine sensitivity in Senegal

Published online by Cambridge University Press:  07 May 2003

J. P. DAILY
Affiliation:
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA
C. ROBERTS
Affiliation:
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA
S. M. THOMAS
Affiliation:
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA
O. NDIR
Affiliation:
Faculty of Medicine and Pharmacy, University Cheikh Anta Diop, Dakar, Senegal
T. DIENG
Affiliation:
Faculty of Medicine and Pharmacy, University Cheikh Anta Diop, Dakar, Senegal
S. MBOUP
Affiliation:
Faculty of Medicine and Pharmacy, University Cheikh Anta Diop, Dakar, Senegal
D. F. WIRTH
Affiliation:
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA

Abstract

Mutations in pfcrt K76T are associated with chloroquine resistance in Plasmodium falciparum. Previous studies of K76T mutations in Senegal reported the association of T76 with in vitro-resistant isolates, but this mutation was also prevalent in chloroquine-sensitive isolates. This suggests involvement of additional genetic loci in modulating chloroquine resistance. Additional pfcrt polymorphisms at codons A220S, Q271E, N326S and R371I have been found in chloroquine-resistant isolates. We wanted to test if sequential acquisition of mutations at these codons leads to in vitro chloroquine resistance. Stepwise accumulation of mutations was not detected, rather there was almost complete linkage between the pfcrt K76T mutation and polymorphisms in these codons. Therefore these additional polymorphisms do not enhance the correlation between pfcrt T76 and chloroquine resistance in Senegal. These data suggest that in vitro chloroquine resistance requires the genetic background of the pfcrt K76T mutation and additional mutations in genetic loci outside the pfcrt gene.

Type
Research Article
Copyright
2003 Cambridge University Press

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